Modares Mechanical Engineering

Modares Mechanical Engineering

Modeling athlete’s heart syndrome caused by hypertension in strength training

Authors
Saeed Torbati 1
Alireza Daneshmehr 2
1 Msc student University of Tehran
2 School of Mechanical Engineering, University of Tehran, Tehran, Iran
Abstract
Persistent strength training can increase ventricular blood pressure and volume and the resultant loading in ventricles of the human heart. It is proved that pressure overload can increase ventricular thickness and volume. In this article, we modeled athlete’s heart syndrome macroscopically arising from pressure overload using continuum mechanics and finite elements methods. We tried to improve previous results by using a more precise geometry and loading and by modifying previous equations. Firstly, we saw that because the left ventricular pressure was more than the right ventricular pressure, increase in myocardium thickness started from the left ventricle and secondly, this increase in myocardium thickness started from lower regions that located far from the right ventricle. Then, it was shown that thicker regions with greater values of the growth multiplier had less stress than regions with less values of the growth multiplier. As time passed and more loading cycles were applied to the endocardium, myocardium thickness increased gradually until the growth multiplier reached its maximum threshold value. Finally, we demonstrated that when the ventricular pressure rises and hypertrophy occurs, residual stresses remain in the myocardium after unloading.
Keywords
Athlete’s heart syndrome
Finite growth
Continuum mechanics
Stem cells
[1] A. L. Baggish, M. J. Wood, Athlete's heart and cardiovascular care of the athlete, Scientific and Clinical Update, Vol. 123, No. 23, pp. 2723-2735, 2011.
[2] S. Göktepe, O. J. Abilez, E. Kuhl, A generic approach towards finite growth with examples of athlete's heart, cardiac dilation, and cardiac wall thickening, Journal of the Mechanics and Physics of Solids, Vol. 58, No. 10, pp. 1661-1680, 2010.
[3] M. K. Rausch, A. Dam, S. Göktepe, O. J. Abilez, E. Kuhl, Computational modeling of growth: Systemic and pulmonary hypertension in the heart, Biomech Model Mechanobiol, Vol. 10, No. 6, pp. 799-811, Dec, 2011.
[4] E. K. Rodriguez, A. Hoger, A. D. McCulloch, Stress-dependent finite growth in soft elastic tissues, Journal of Biomechanics, Vol. 27, No. 4, pp. 455-467, 1994.
[5] E. Kuhl, Growing matter: A review of growth in living systems, Journal of the Mechanical Behavior of Biomedical Materials, Vol. 29, pp. 529-43, Jan, 2014.
[6] A. M. Zöllner, M. A. Holland, K. S. Honda, A. K. Gosain, E. Kuhl, Growth on demand: Reviewing the mechanobiology of stretched skin, Journal of the Mechanical Behavior of Biomedical Materials, Vol. 28, pp. 495-509, 2013/12/01/, 2013.
[7] J. Bonet, R. D. Wood, Nonlinear Continuum Mechanics for Finite Element Analysis, 2nd ed., pp. 157-159, United States of America Cambridge University Press, 2008.
[8] B. Fereidoonnezhad, R. Naghdabadi, S. Sohrabpour, G. A. Holzapfel, A mechanobiological model for damage-induced growth in arterial tissue with application to in-stent restenosis, Journal of the Mechanics and Physics of Solids, Vol. 101, No. Supplement C, pp. 311-327, 2017/01/01/, 2017.
[9] A. Khalilimeybodi, Modeling Cardiac Growth by Considering the Effects of Biomechanical and Biochemical Factors Simultaneously, Doctor of Philosophy Thesis, School of Mechanical Engineering, University of Tehran, Tehran, 2017. Persian (in Persian فارسی(
[10] A. I. Hassaballah, M. A. Hassan, A. N. Mardi, M. Hamdi, An inverse finite element method for determining the tissue compressibility of human left ventricular wall during the cardiac cycle, Plos One, Vol. 8, No. 12, pp. e82703, 2013.
[11] E. Kuhl, A. Menzel, P. Steinmann, Computational modeling of growth, Computational Mechanics, Vol. 32, No. 1-2, pp. 71-88, 2003.
[12] G. A. Holzapfel, Nonlinear Solid Mechanics A Continuum Approach for Engineering, pp. 1-52, England: Wiley, 2000.
Modares Mechanical Engineering
Volume 18, Issue 3
May 2018
Pages 389-394